The following description is provided to assist the understanding of the reader. None of the information provided or the references cited are admitted to be prior art to the present invention.
Burn trauma causes approximately two million injuries, 100.000 hospital admissions, and 10,000 deaths every year in the United States. In the past, many victims did not survive the initial resuscitation period. Current survival rates and clinical outcomes have progressively improved with the advent of aggressive burn wound excision techniques, graft therapy, and superior intensive care facilities, along with a better understanding of post-burn physiological factors and fluid requirements.
Systemic injury, such as the dysfunction or failure of an organ secondary to a severe burn injury and which is not attributable to the burn injury, remains a continuing source of morbidity and mortality. A severe burn is associated with release of inflammatory mediators which ultimately cause local and distant pathophysiological effects. Mediators including Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) are increased in affected tissue, which are implicated in pathophysiological events observed in burn patients.
Free radicals have been found to have beneficial effects on antimicrobial action and wound healing. However, following a burn, there is an enormous production of ROS which is harmful and implicated in inflammation, systemic inflammatory response syndrome, immunosuppression, infection and sepsis, tissue damage and multiple organ failure. Thus, clinical response to burn is dependent on the balance between production of free radicals and its detoxification.